Cases reported "Uremia"

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1/7. Severe proximal myopathy in advanced renal failure. Diagnosis and management.

    Myopathies encountered in uremic patients may have different pathogenetic mechanisms and treatment. Secondary hyperparathyroidism may cause uremic myopathy responding to specific treatment. This study aimed at presenting a case illustrative of the clinical features, diagnosis and management of uremic parathyroid myopathy. A 66-year old man with renal failure from membranous nephropathy developed sensory signs of uremic neuropathy and progressive painless weakness of the pelvic girdle muscles bilaterally. Motor nerve conduction velocity was normal, electromyogram was consistent with a myopathic pattern, while muscle biopsy showed a pattern of atrophy more consistent with a neuropathic pattern. Serological tests for collagen vascular diseases and hyperthyroidism were negative, while serum muscle enzymes were not elevated and serum phosphate levels were not low. serum parathyroid hormone level was grossly elevated, while serum calcium was mildly elevated in a small fraction of the measurements, serum alkaline phosphatase showed a progressive rise and skeletal bone survey did not disclose osteopenia or signs of parathyroid bone disease. A course of calcitriol failed to improve the myopathy, which responded promptly and dramatically to parathyroidectomy. Uremic parathyroid myopathy, which has a characteristic clinical picture, must be differentiated from other neuropathic or myopathic conditions that require specific treatments. Progressive parathyroid myopathy is, by itself, an indication for parathyroidectomy, which is curative in this case.
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2/7. Lactic acidosis with hypoglycemia and hyperammonemia observed in two uremic patients during calcium hopantenate treatment.

    calcium hopantenate (HOPA), a drug for treating symptoms of cerebrovascular disease, is a derivative of gamma-amino butyric acid and is also an analog of pantothenic acid. It is speculated that calcium hopantenate may affect lactate generation, glucose metabolism, and ammonia disposal through the inhibition of pantothenic acid metabolism. We report two uremic patients with complaints of consciousness disturbance with lactic acidosis, hypoglycemia and hyperammonemia. HOPA is mainly excreted with urine. Severe accumulation of HOPA, documented at the onset of unconsciousness in our uremic cases, might be responsible for marked inhibition of pantothenic acid metabolism.
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keywords = vascular disease
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3/7. Severe reversible azotemia from captopril therapy. Report of three cases and review of the literature.

    We saw three cases of severe reversible azotemia secondary to captopril therapy in hypertension. All patients had extensive peripheral vascular disease involving the renal arteries, and two patients (patients 2 and 3) had high levels of peripheral plasma renin activity. The azotemia occurred approximately two weeks after exposure to captopril, and fever, a maculopapular pruritic cutaneous rash, and eosinophilia developed in two patients (patients 2 and 3). The cause of the azotemia in our patients is not clearly known, since renal biopsies were not performed. The most likely cause for the azotemia was volume contraction with reduction in the glomerular filtration rate, although a direct insult to the kidney could not be excluded.
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keywords = vascular disease
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4/7. Amyloid vascular disease and contracted kidneys--report of a case with review of literature.

    A case of systemic amyloidosis associated with bronchiectasis is presented. At necropsy, contracted kidneys and centrilobular necrosis of the liver were observed. Systemic blood vessels had heavy deposition of amyloid, and the possibility of visceral ischemia and the development of contracted kidneys due to amyloid vascular disease as a pathogenetic relationship, was discussed against the background of a review of the literature.
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keywords = vascular disease
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5/7. Focal neurologic signs associated with hyperkalemia.

    A patient with end-stage renal disease had a flaccid hemiparesis in conjunction with severe hyperkalemia. The hemiparesis resolved with treatment of the hyperkalemia. The patient was later found to have extracranial vascular disease, and we propose that a severe metabolic abnormality associated with an area of relative cerebral ischemia caused the reversible neurologic deficit.
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keywords = vascular disease
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6/7. Bilateral ureteral obstruction following aortic bypass surgery.

    A patient developed azotemia from bilateral ureteral obstruction due to retroperitoneal fibrosis after placement of an aortofemoral bypass graft for atherosclerosis in that region. This complication of abdominal vascular prosthesis may be more common than is presently recognized; especially since the patient may remain asymptomatic till an advanced degree to azotemia supervenes. At that time irreversible damage to the kidney may occur. Furthermore, silent damage in the kidneys may be attributed to other causes in these patients who may also have severe vascular disease or prostatic disease. When a gradually increasing azotemia is seen in a patient who had aortofemoral bypass surgery, ureteral obstruction from retroperitoneal fibrosis should be one of the main considerations in the differential diagnosis. Computed tomography, isotope renography and sonography may be helpful in making an early diagnosis and should be a part of the postoperative follow-up care in these patients.
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keywords = vascular disease
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7/7. Case report: azotemia secondary to enalapril and diuretic use and the diagnosis of renovascular hypertension.

    When administered to a 45-year-old woman who was ill with severe hypertension, combined enalapril and hydrochlorothiazide therapy resulted in acute renal failure, leading to a successful search for renal artery stenosis. Acute renal failure as an adverse reaction to enalapril therapy occurs in approximately 20% of patients with secondary hypertension from renovascular disease. On the other hand, in a group of essential hypertensives this occurs at a rate of approximately 0.2%. Thus, a likelihood ratio of 100 is produced, and given the prevalence of renovascular hypertension of approximately 2% in all hypertensives, a posterior probability of 0.67 can be calculated. The occurrence of this adverse effect should indicate that a diagnostic work-up to rule out renovascular hypertension in such patients should be pursued. The sensitivity and specificity of this "test" are 0.20 and 0.998, respectively. This illustrates that the mathematic aids in decision theory need not be applied solely to those more traditional aspects of diagnostic testing, but may be useful in other situations as well.
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